To date, endothelial dysfunction is defined by a constellation of phenotypes including up-regulation of pro-inflammatory pathways, enhanced thrombogenicity, increased reactive oxygen species and reduced NO synthesis/bioavailability1, 2. Our lab has focused on the latter pathway by understanding how endothelial nitric oxide synthase (eNOS), the exclusive source of endothelial derived NO as a relaxing factor for smooth muscle, is regulated and these studies have led to the discovery of additional pathways that regulate several aspects of endothelial cell biology and function3. Thus, the central goal for this grant is to integrate advances derived from our previous work on eNOS to explore a broader range of pathways that can improve endothelial and vascular health.

Public Health Relevance

This research is relevant to public health since we have endothelial dysfunction occurs in the blood vessels of patients with cardiovascular disease. Understanding how nitric oxide is released from blood vessels can lead to new therapeutic approaches for heart disease.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Unknown (R35)
Project #
3R35HL139945-01S1
Application #
9693565
Study Section
Program Officer
Gao, Yunling
Project Start
2018-01-01
Project End
2024-12-31
Budget Start
2018-09-10
Budget End
2018-12-31
Support Year
1
Fiscal Year
2018
Total Cost
Indirect Cost
Name
Yale University
Department
Pharmacology
Type
Schools of Medicine
DUNS #
043207562
City
New Haven
State
CT
Country
United States
Zip Code
06520